Glaucoma is, after diabetes, the second leading cause of blindness in the world. Vision loss as a result of glaucoma involves both central and peripheral vision and has a major impact on the ability of people to live independent lives.
Glaucoma is an eye disease caused by an elevated pressure within the eyeball, which damages the optic nerve and eventually produces total and irreversible loss of sight. It is produced by a failure in the natural drainage system of the eye, resulting in a reduced capacity for draining aqueous humor, which is a fluid that is produced continuously inside the eye as part of its normal functioning. As a result of this failure in the natural drainage system, fluid outflow is reduced and therefore the pressure within the eyeball is increased.
The Glaucoma is an optic neuropathy (a disorder of the optic nerve) caused by an elevated intraocular pressure. The high pressure inside the eye compresses the outlet of the optic nerve (papilla) causing changes in its appearance and in the visual function (increase of the optic cup and alterations to the visual field). If the pressure remains increased over a prolonged period of time, a complete and irreversible vision loss takes place.
The intraocular pressure is maintained by a balance between the production and the outflow of aqueous humor. Aqueous humor is a fluid produced by the ciliary body in the posterior chamber of the eye at a rate of approximately 3 to 5 microliters per minute. The fluid produced then passes through the pupillary opening of the iris into the anterior chamber of the eye. Once in the anterior chamber, the fluid leaves the eye through the junction between the cornea and the iris (iridocorneal angle) through a filter called Trabecula, which is composed by collagen bundles arranged in three-dimensional structure similar to a sieve. From that point the aqueous humor goes to the Schlemm's canal and then to the episcleral veins.
As the eye is a closed and inelastic sphere, the production and outflow of aqueous humor necessarily have to be equal. This causes a pressure inside the eye that is determined by the amount of fluid produced and the capacity of outflow that it has. In normal conditions, the intraocular pressure ranges between 10 and 21 mm Hg.
If the production of aqueous humor increases, the intraocular pressure will increase to achieve greater outflow. If the outflow resistance increases, the intraocular pressure will increase to increment the outflow. Both scenarios will increase intraocular pressure and may cause glaucoma, being much more frequent the increase in the outflow resistance.
The resistance to the outflow of aqueous humor may be increased by several factors. Thus, in the “primary open angle glaucoma (POAG)” (responsible for 85% of glaucoma), the abnormal resistance is produced along the outer aspect of the trabecular meshwork and the inner wall of the Schlemm's canal. In the “primary angle closure glaucoma (PACG)” the resistance increases by mechanical blocking of the angle and in “secondary glaucoma” due to diverse motives such as inflammatory waste deposits, vascularization of the area, pigment blocking, etc.
Whatever the factor that produces it, increased intraocular pressure compresses the outlet of the optic nerve and interferes in its vascularization, causing the death of nerve cells that carry the visual stimulus to the brain, producing alterations in the visual field and, in advanced cases, total and irreversible blindness.
The only therapeutic approach currently available for glaucoma is to lower intraocular pressure.
The clinical treatment of glaucoma is done step by step, the first step being the medical treatment either by oral means or with drops.
The drugs work by reducing aqueous humor production or by facilitating its outflow. The drugs that are currently available can have many side effects, some serious that include congestive heart failure, respiratory distress, hypertension, depression, kidney stones, aplastic anemia, sexual dysfunction and death. Compliance with medication is also a major problem, being estimated that more than half of glaucoma patients do not follow their dosing schedules correctly.
While medications work, they will be the recommended treatment, but often are not sufficient to maintain a safe intraocular pressure and surgery is needed. The most frequent surgeries are Trabeculoplasty and Trabeculectomy.
In laser trabeculoplasty, thermal energy from a laser is applied to a number of noncontiguous spots in the trabecular meshwork. It is believed that the laser energy somehow stimulates the metabolism of the trabecular cells and changes the extracellular material of the trabecular meshwork. In approximately 80% of patients, aqueous outflow is increased and the pressure decreases. However, the effect often is not long lasting and 50% of patients develop hypertension again in five years.
In addition, laser trabeculoplasty is not an effective treatment for primary open angle glaucoma (POAG) in patients of less than fifty years old nor is effective for glaucoma due to angle closure and many secondary glaucomas.
If laser trabeculoplasty does not reduce the pressure to the desired level, filtering surgery is then performed.
The most commonly used filtering procedure is the trabeculectomy. In a trabeculectomy an incision is made in the conjunctiva, which is the transparent tissue that covers the sclera. The conjunctival tissue is lifted and a scleral flap of approximately 4×4 mm is made with a depth of 50% of the scleral thickness and is lamellar dissected up to 1 mm into the cornea. The anterior chamber is entered beneath the scleral flap and a section of the deep sclera and trabecular meshwork is excised. The scleral flap is loosely sewn back into place and conjunctival incision is closed well. Postoperatively, the aqueous humor passes through the hole beneath the scleral flap and goes to the sub conjunctival space where it forms a blister from where it passes to the blood vessels of the conjunctiva or traverses the conjunctiva to the surface.
Trabeculectomy is associated with many problems, among them, the fibroblasts that are present in the episclera proliferate, migrate and can scar the scleral flap, failures in scarring may occur, particularly in children and young adults. Of the eyes that have had an initially successful trabeculectomy, 80% will stop filtering in a period of 3 to 5 years after surgery. To minimize fibrosis, surgeons are now are applying antifibrotic agents such as mitomycin C (MMC) and 5-fluorouracil (5-FU) to the scleral flap at the time of surgery. The use of these agents has increased the success rate of trabeculectomy, but also has increased its complications.
When trabeculectomy does not successfully lower the eye pressure, the next surgical step is often an aqueous shunt valve. This device consists of a silicone tube that is attached at one end to a plastic plaque (polypropylene or other synthetic) with valve shape that is sewn to the ocular equator or a tittle after this point and the other end of the silicone tube is introduced into the anterior chamber through a hole made in the corneal limbus. The outer portion of the tube is covered with sclera or pericardium from donor, it is all covered with the conjunctiva and the incision is closed. There are many problems with the current technology of these aqueous shunt valves, including bad scarring, valve failure, hypotony and infection.
In the year 1999 the company Optonol patented a tubular filtering device, not valved for the control of intraocular pressure in glaucoma (Patent U.S. Pat. No. 5,968,058). This device was a small stainless steel tube that, once placed in the corneal limbus, allowed the flow of aqueous humor through the tube from the anterior chamber to an intrascleral space and from there to the sub conjunctival space. Since 2002, the company Alcon sells this device under the name of Ex-Press.
The implantation of these permits less invasive surgeries compared to the trabeculectomy, because allows the aqueous humor outflow without the need of extracting a segment of the trabecula or performing an iridectomy.
Several studies have reported on the effectiveness of these devices to significantly reduce intraocular pressure, but also report of complications, been the most common frequent flat chamber (excessive loss of eye pressure) and bleeding in anterior chamber, which is believed may be related with the anchoring system.
All the surgical techniques to reduce intraocular pressure seek to create a new drainage pathway for aqueous humor that can replace the obstructed normal path, with the fewest amount of possible complications.
However, the current treatments and surgical techniques may present complications such as:                May get obstructed or stop functioning in a short period of time.        May produce an excessive loss of pressure in the eye.        May produce intraocular bleeding and associated complications.        May produce infections.        May require complex and aggressive surgery.        
In this sense, the flat drainage device for the control of intraocular pressure in glaucoma presented in this document has significant advantages over existing alternatives for the surgical treatment of this illness.